Role of neural mechanisms
Biological explanations to
eating behaviour
Evolutionary explanations
Role of neural mechanisms
in eating behaviour
• Eating behaviour = ingestive behaviour
The process by which the
• Homeostasis
– if we are hot – we sweat
– if we are dehydrated – thirsts
– If we need food – hunger
body maintains a constant
internal environment
• Homeostasis is maintained via a negative feedback
loop: this assumes that all body variables have a set
point (or range)
• The digestive tract and the hypothalamus play a
significant role in eating behaviour.
Body weight
• Each individual has a set point and their
weight is regulated around that set point
• Body regulates hunger based possibly on
– Fat stores (lipostatic hypothesis)
– Glucose levels (glucostatic hypothesis)
– Cellular energy – adenosine trisophate (ATP) is a
product of the breakdown of macronutrients (fats,
carbohydrates and proteins) and considered
important for the regulation and maintenance of
homeostasis
The hypothalamus
• Patient with tumours in the hypothalamus tend
to become obese
• Methods used to research hypothalamus
– Lesioning in animals
– Investigation of feeding
patterns after brain damage
– Effects of neurotransmitters
introduced into parts of brain
– Impact of drugs on eating
– Use of fMRI (Functional
Magnetic Resonance Imaging)
Dual-Centre Theory of feeding
behaviour
• 2 areas of the hypothalamus involved in
eating behaviour
– Ventro Medial Hypothalamus (VMH) as a "satiety
center"
– Lateral Hypothalamus (LH) as a "Hunger center".
• NOTE: VMH and LH are also called VMN and
LN (N stands for NUCLEUS!!!)
Dual-Centre Theory of feeding behaviour
The lateral nucleus of the
hypothalamus
• Contains the
feeding centre
• This initiates eating.
• It responds to
decreased blood
glucose and
increase in ghrelin a
hormone released
from the stomach
when it is empty.
Ventro medial
nucleus (VMN)of the
hypothalamus
• Contains the satiety
centre.
• This inhibits eating
behaviour when we are
full.
• Responds to
– an increase in blood
glucose,
– a decrease in ghrelin and
to CCK, a hormone
released when food is
detected in the
duodenum
– leptin a long term satiety
signal released by fat
cells.
Role of hypothalamus - evidence
• Aphagia (failure to eat when hungry) can be
caused by damage to the LH
• Rats whose VMH had been lesioned developed
overeating and obesity
• However, Gold (1973) found that lesions
restricted to the VMH alone did NOT result in
hyperphagia and only produced overeating when
they included other areas such as the
parvoventricular nucleus!
• However, subsequent research has failed to
replicate Gold’s findings...
Role of ghrelin - evidence
• Cummings et al (2004) monitored PPs’ ghrelin levels every 5 minutes
• PPs had to assess their level of hunger every 30 mins.
• In 5 of the 6 participants there was a significant correlation between
ghrelin levels, emptiness of the stomach and hunger.
• The results support the theory of the role of ghrelin in eating
behaviour
• AO3: The study used a small sample limiting how far the findings can
be generalised and it is likely that the participant’s subjective
judgements of hunger were influenced by expectations of food
based on meal times (cultural factors rather than biological factors)
• Ghrelin injections result in increased food intake in animals
• Gastric bands used in treating obesity reduce ghrelin secretion.
Role of neurotransmitters
• 3 main neurotransmitters are found to influence
appetite:
– Catecholamines (dopamine, norepinephrine, and
epinephrine): sympathomimetic "fight-or-flight"
hormones that are released by the adrenal glands in
response to stress
– Serotonin: found extensively in the gastrointestinal
tract, it activates the muscles used for feeding. Is also
associated to aggression and “happiness”
– Peptides: short polymers formed from the linking, in a
defined order, of α-amino acids
Neurotransmitters
that increase food intake
• Norepinephrine (NE) – injections of NE in hypothalamus
– can stimulate feeding if injected into the paraventricular
nucleus
– Can reduce feeding if injected into the perfornical area
• Neuropeptide Y (33 amino acid peptide)– high
concentrations in the paraventricular hypothalamus and
perfornical hypothalamus.
– Rats injected with neuropeptide Y continue eating large
amounts of food even when full
– It also seems to cause a preference for carbohydrates
• Galanin (29 amino acid peptide)- particularly found in the
paraventricular hypothalamus.
– Injections of galanin into rats cause an increase of food intake
and a preference for fats rather than carbohydrates
Marie et al (2005)
role of neuropeptide Y
• Genetically manipulated mice so that they did
not produce neuropeptide Y
• Found no subsequent decrease in their
feeding behaviour!!
• However, injections of NPY cause hunger...
• ...May be due to an experimental artefact,
because of the unexpected intake of NPY in
experimental conditions (through injection)
Neurotransmitters and modulators
that decrease food intake
• Cholecystokinin (CCK) – endogenous 33 amino acid
peptide that is released into bloodstream during meals
– Causes reduction in appetite and satiation
– Suppresses weight gain
• Bombesin – peptide found to reduce food intake in rats
• Corticotropin-Releasing Hormone (CRH) – 41 amino acid
peptide produced in the paraventricular hypothalamus and
other regions of brain that reduces food intake
• Serotonin (5HT) – neurotransmitter which decreases food
intake.
KEY WORDS – matching exercise
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Homeostasis
Negative feedback loop
Set point
Lipostatic hypothesis
Glucostatic hypothesis
adenosine trisophate
(ATP)
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Lateral Nucleus
Ventro Medial Nucleus
Ghrelin
CCK
Leptin
Neuropeptide Y (NPY)
Impact of drugs on eating behaviour
• Nicotine – decreases food intake.
– Smokers generally weigh 3 kg less than non-smokers
(US Department of Health and Human Services, 1990)
– Ogden (1994) some dieters use smoking as a weightloss strategy and those who stop smoking increase
their calorie intake, especially from sweet foods
• Amphetamines - have a dramatic suppressant
impact on both subjective hunger and food intake
• Marijuana – increases hunger and food intake
Impact of drugs on eating behaviour
• Alcohol – influences food intake in contradictory
ways
– Some studies indicate it can have a weak inhibitory
effect
– Others show it can stimulate hunger
• Anti-psychotic drugs – both lithium and
chloropromazine cause considerable weight gain
• Tricyclic anti-depressants – cause cravings for
sweet food and weight gain
• Selective Serotonin Reuptake Inhibitors (SRRIs) –
used for patients with depression, might promote
weight loss...
Impact of drugs on eating behaviour
• Analgesics – used for pain relief
– Naloxone can trigger deceased food intake
– Morphine has also a weak depressant effect on
appetite
• Appetite-suppressant drugs
– have a consistent depressant effect on hunger and
reduce food intake
– Have been removed from the market because
linked to heart problems
Does it increase or decrease hunger?
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•
•
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Morphine DECREASE
Anti-psychotic drugs INCREASE
Tricyclic anti-depressants INCREASE
Selective Serotonin Reuptake
Inhibitors (SRRIs) DECREASE
• Naloxone DECREASE
• Alcohol BOTH!
• Appetite-suppressant drugs DECREASE
issues
debates
approaches
• Ethical issues with non-human animals
• Is the biological approach reductionist?
• Free will vs determinism (can biological drives be
overridden?)
• Compare and contrast explanations to eating
behaviour
• Biological,
• Learning (Behaviourist)
• Cognitive
• Social
Evaluation of neural mechanisms and
eating behaviour
+Reflection on people’s experience of hunger\satiety
+Insight into brain chemicals – could be used to develop
medical interventions to help change what we eat
+Provides explanation of some differences in eating behaviour
+Studies such as those involving lesions to the LH and VMH in
rats have supported the role of the hypothalamus in
regulating eating behaviour
+Studies involving electrical stimulation of these centres have
confirmed their role in feeding and satiety.
+Such studies provide sound scientific evidence but there is
the issue of extrapolating finding from rats to humans.
+Research evidence
• Cumming et al, 2004 - ghrelin
Cont.
-Reductionism: focus exclusively on biological aspects of
hunger and satiety
-Biological determinism: focus exclusively on the role of
nature and no space left to choice and cultural and social
influences
-there is substantial and convincing evidence that social,
cultural and psychological factors affect our eating
behaviours as is evident from psychological explanations of
eating disorders
-Use of animals in research implies lack of generalisability
-Highly controlled lab experiments may lack ecological validity
-Physiological drives can be overriden (eg desire to loose
weight; dislike of certain foods; fear of losing control; social
cues to continue eating; food availability)
Outline and evaluate the role of neural
mechanisms involved in controlled eating and
satiation(25 marks)
• AO1:
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Intro: homeostasis; negative feedback loop; set point
Lipostatic and glucostatic hypotheses
describe dual centre model (diagram will be also credited);
Role of LH and VMH;
neurotransmitters and hormones involved in eating regulation (ghrelin; CKK;
leptin; norepinephrine; Neuropeptide Y...)
• AO2:
– research evidence for effects of hormones + contrasting evidence (eg Cummings
et al, 2004 ghrelin AND Marie et, 2005 NEY al OR Gold, 1973 VMH lesioning) (4)
– Impact of drugs (eg alcohol, anti-depressants...) on appetite confirms biological
basis of eating behaviour
– I: ethics with non-himan PPs; reductionism
– D: free will vs determinism; nature vs nurture
– A: biological vs social, behaviourist, psychodynamic
• AO3
– Lack of ecological validity
– Lack of generalisability
– Sampling issues (eg Cummings et al, 2004)